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Lobular Breast Cancer Different Disease, Different Algorithms?

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Lobular Breast Cancer Different Disease, Different Algorithms? Lobular Breast Cancer Different Disease, Different Algorithms? a b,c, Anita Mamtani, MD , Tari A. King, MD * KEYWORDS Invasive lobular carcinoma E-cadherin The Cancer Genome Analysis Breast conservation Mastectomy Chemotherapy Aromatase inhibitors KEY POINTS Invasive lobular breast cancer is a biologically unique entity, distinct from invasive ductal cancer. The characteristic molecular features of invasive lobular carcinoma (ILC) include its largely ER-positive and low-grade nature, and loss of E-cadherin protein expression. Tumor biology is of key importance in designing treatment approaches. Harnessing the growing knowledge of the molecular features inherent to lobular cancer holds promise for the next generation of tailored therapies. INTRODUCTION Invasive lobular carcinoma (ILC) is the second most common histologic form of breast cancer, comprising 10% to 15% of invasive tumors.1 ILC is now recognized as a biologically distinct disease from the more common invasive ductal carcinoma (IDC), with a unique molecular pathogenesis and consequential implications on diagnosis and treatment. An understanding of these differences is of utmost importance to tailor management strategies. Ongoing investigations of the genomic basis of breast cancer are paving the road for novel approaches to treatment of ILC. EPIDEMIOLOGY The mean age of diagnosis of ILC is 57 years.2 Risk factors include age at menarche, age at first birth, and use of hormone therapy, emphasizing the role of estrogen The authors have nothing to disclose. a Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Bos- ton, MA, USA; b Department of Surgery, Brigham and Women’s Hospital, 75 Francis Street, Bos- ton MA 02215, USA; c Breast Oncology Program, Dana-Farber/Brigham and Women’s Cancer Center, 450 Brookline Avenue, Boston, MA 02215, USA * Corresponding author. E-mail address: [email protected] Surg Oncol Clin N Am 27 (2018) 81–94 http://dx.doi.org/10.1016/j.soc.2017.07.005 surgonc.theclinics.com 1055-3207/18/ª 2017 Elsevier Inc. All rights reserved. 82 Mamtani & King exposure in pathogenesis. This relationship is also observed for most IDCs, but is more pronounced for ILC.3 The incidence of ILC in the Western world has generally mirrored trends in use of hormone replacement therapy, with a steep increase be- tween 1975 and 2000 and a decline between 2000 and 2004, but now increasing since 2005 with an unclear cause.4 Hereditary ILC is uncommon, but may be seen as a secondary tumor in families with hereditary diffuse gastric cancer syndrome, caused by a germline mutation in the tumor suppressor gene, CDH1. ILC otherwise accounts for a minority of cancers asso- ciated with known susceptibility genes, comprising less than 10% of cancers in pa- tients with BRCA2 mutations, and less than 5% of cancers in patients with BRCA1 or TP53 mutations.5 HISTOLOGY Classic ILC is histologically characterized by discohesive cells infiltrating the breast stroma in a single-file pattern2 with a limited host inflammatory response (Fig. 1A).6 Observed loss of membranous E-cadherin staining by immunohistochemistry may be a useful adjunct to confirm the diagnosis (see Fig. 1B). Several nonclassic forms of ILC have also been described, distinguished by morphology (alveolar, solid, dispersed, trabecular, and mixed) and cytology (apocrine, pleomorphic, signet ring, histiocytoid, and tubulolobular).5 These variant forms show the typical cytologic Fig. 1. (A) Hematoxylin and eosin staining, 10Â and 20Â magnifications, depicting the classic “single-file” morphology of ILC. (B) Immunohistochemistry of paraffin-embedded breast cancer tissue showing characteristic loss of membranous E-cadherin in lobular carcinoma. (Courtesy of Dr Stuart J. Schnitt, MD, Chief of Breast Oncologic Pathology, Dana-Farber/Brigham and Women’s Cancer Center; Associate Director, Dana-Farber Cancer Institute/Brigham and Women’s Hospital Breast Oncology Program; Professor of Pathology, Harvard Medical School.) Lobular Breast Cancer 83 features of classic ILC, but display differing growth patterns. In the alveolar variant, cells are organized in globular arrangements, whereas the solid variant displays sheets of uniform cells with high frequency of mitoses. Conversely, the low-grade tubulolob- ular variant displays linear cells with tubular glands. The most aggressive pleomorphic variant of ILC exhibits greater atypia, nuclear pleomorphism, and frequent mitoses, with variable degrees of apocrine differentiation.2 Associated lobular neoplasia (LN), which refers to the noninvasive proliferative lobular lesions inclusive of atypical lobular hyperplasia and lobular carcinoma in situ (LCIS), is observed in more than 50% of classic ILCs.2 The reported incidence of pure LN ranges from 0.5% to 4%,2 and typically presents in younger women than does ILC. Histologically, LN displays pagetoid terminal duct involvement in more than 70% of cases. There exist 2 types of LN, type A (classic cellular features) and type B (larger, atypical cells with prominent nucleoli), with a small subgroup displaying pleomorphic cells with apocrine features and more aggressive biology, termed pleo- morphic LCIS.2 LN is considered a risk factor for the subsequent development of invasive cancer of either the ductal or the lobular phenotype. The increased risk ranges from 1% to 2% per year and is conferred equally to both breasts.7 Recent work demonstrating shared molecular alterations between LCIS and synchronous ILCs in a significant proportion of cases has also reopened the notion that some LCIS lesions may behave as nono- bligate precursors of ILC.2 MOLECULAR BIOLOGY More than 90% of ILCs are estrogen receptor (ER) positive and they are largely clas- sified as luminal A at the level of the transcriptome, although this proportion is lower in more aggressive variants,5 with highest rates of ER positivity observed in the classic form and alveolar variants, and lowest rates of ER positivity observed in pleomorphic ILCs (10%).2 HER2 overexpression is rare, seen in only 3% to 5% of classic ILCs, but present in up to 80% of the more aggressive pleomorphic subgroup.2,4 Loss of E-cadherin expression is the most consistently reported hallmark feature of ILC (see Fig. 1B), demonstrated in up to 90% of cases, and thought to play a crucial role in pathogenesis.2 E-cadherin is a calcium-dependent transmembrane protein involved in adherens-type junctions between epithelial cells, the loss of which predis- poses to neoplastic proliferation. E-cadherin dysregulation results from somatic muta- tions in the CDH1 gene on chromosome 16q22.1, reported in 30% to 80% of ILCs, as well as by loss of heterozygosity at the CDH1 locus.2,8 However, E-cadherin positivity does not, by itself, exclude a lobular neoplasm, and not all ILCs harbor CDH1 muta- tions. Other markers frequently expressed in ILC include GCDFP-15, seen in up to 90% of pleomorphic and signet ring subtypes,2 cyclin D1 (80%), cathepsin D (86%), Bcl-2 (89%), and Ck 34BetaE12.2 In the Cancer Genome Analysis study, mutations in several key genes were found more frequently in ILC as compared with IDC, including CDH1 (63% in ILC vs 2% in IDC), P1K3CA (48% vs 33%), FOXA1 (7% vs 2%), RUNX1 (10% vs 3%), and TBX3 (9% vs 2%), respectively.4 Conversely, GATA3 mutations were enriched in IDC (5% in ILC vs 13% in IDC). Importantly, when the analysis was limited to luminal A cancers, several alterations remained significantly more common among ILCs versus IDCs, as summarized in Table 1.4 A later analysis of 417 ILCs by Desmedt and colleagues9 reported that more than half of the cases contained a mutation in PIK3CA, PTEN, or AKT1, and there was also an increased frequency of HER2, HER3, FOXA1, and ESR1 alterations. 84 Mamtani & King Table 1 Genomic alterations seen with increased frequency in luminal A lobular cancers (n 5 106) versus luminal A ductal cancers (n 5 201) in The Cancer Genome Analysis study Gene Q Valuea CDH1 1.4EÀ30 FOX1A 0.065 PIK3CA Not stated PTEN 0.035 RUNX1 Not stated TBX3 0.05 a Depicted “q value” represents a P value that is adjusted for the proportion of expected false positives. Data from Ciriello G, Gatza ML, Beck AH, et al. Comprehensive molecular portraits of invasive lobular breast cancer. Cell 2015;163:506–19. CLINICAL PRESENTATION AND DIAGNOSIS ILC may pose a diagnostic challenge because of its inherently insidious and infiltrative growth pattern. Although some patients present with an ill-defined palpable mass, others may display only vague skin thickening or diffuse nodularity, or disease may be clinically occult.2 In keeping with their indolent phenotype, ILCs are not frequently associated with calcifications and have an innately discohesive growth pattern. As such, ILCs frequently display a scattered radiological appearance. Compared with IDCs, ILCs are more often mammographically occult, with sensitivity as low as 57% to 76%2 and false negative rates as high as 25%.10 These tumors also tend to be poorly circumscribed, which may limit the accuracy of both breast and axillary ultra- sound. The sensitivity of ultrasound-guided fine-needle aspiration of lymph nodes in ILC is low, reported to be less than 40% in cases of pure ILC.11,12 Table 2 summarizes reported correlations between pathologic and radiologic tumor size as visualized by mammogram, ultrasound, and MRI.13–17 The utility of preoperative MRI in the workup and staging of lobular cancers remains controversial, with mixed data on resultant rates of mastectomy or reexcision after breast conservation. A recent large meta-analysis found that preoperative MRI in- creases rates of mastectomy for all cancer histologies, suggesting an unfavorable overestimation of the extent of disease.18 On subset analysis of 766 ILC patients, although there was some reduction in the rate of reexcision after breast-conserving Table 2 Correlation of pathologic and radiologic tumor size of lobular carcinomas Study Mammogram Ultrasound MRI Boetes et al,16 2004 (n 5 34) 0.34 0.24 0.81 Francis et al,13 2001 (n 5 22) 0.79 0.56 0.87 Kepple et al,17 2005 (n 5 29) — 0.71 0.88 Kneeshaw et al,15 2003 (n 5 21) — — 0.86 Munot et al,14 2002 (n 5 20) 0.66 0.67 0.97 All values are reported as correlation coefficient.
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